CDK9 Antibody
- Known as:
- CDK9 Antibody
- Catalog number:
- 32311
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CDK9 Antibody
Related genes to: CDK9 Antibody
- Gene:
- CDK9 NIH gene
- Name:
- cyclin dependent kinase 9
- Previous symbol:
- CDC2L4
- Synonyms:
- PITALRE, C-2k, TAK
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-29
- Date modifiied:
- 2016-10-05
Related products to: CDK9 Antibody
Related articles to: CDK9 Antibody
- Previous research has predominantly focused on the regulatory role of lncRNA in gene silencing by interacting with the Polycomb repressive complex 2 (PRC2), but its direct role as a transcriptional activator remains less well characterized. Here, our study reveals a novel regulatory mechanism of , which facilitates prostate cancer (PCa) progression by enhancing transcription elongation. Integrating ChIRP-seq, RNA-seq, and ChIP-seq, we found that HOTAIR co-localizes with AR and facilitates the interaction between CDK9 and Pol II. This function requires the 1-442 nt region and intact RNA, as deletion or RNase treatment disrupts the interaction. Re-expression of full-length HOTAIR, but not the deletion mutant, restores nascent transcription of target genes; conversely, CDK9 inhibition suppresses this elongation effect. We identified and as functional downstream targets; ectopic expression of either rescues colony formation and invasive migration upon depletion. knockdown reduced Ser2P and Ser5P signals at target loci, yet RNA pull-down showed no direct binding to Pol II Ser5P, implying that any effect on initiation is indirect. This elongation activity operates in both AR-positive and AR-negative cells, with AR acting as a context-specific recruiter. Collectively, these findings support a model in which functions as an elongation activator and suggest potential therapeutic targets in prostate cancer. - Source: PubMed
Publication date: 2026/09/10
Qian YuyangWang BoSu GuangsongLi PengZhao ZhenhaoJiang YuanZhang LeiZhao ZhongfangLi Mulin JunShi JiandangHuang DandanLu Wange - Cohesin organizes 3D genome architecture yet its acute depletion in vitro minimally affects transcription, leaving its regulatory role puzzling. We hypothesized that cohesin function is relevant when first encounters chromatin after mitosis. Using in vivo labeling and cell-cycle synchronization in human cells, we demonstrate that cohesin complexes persist through mitosis. This inherited pool dominates over newly translated cohesin during telophase-G1, highlighting the relevance of such transmission. Acute depletion of cohesin Rad21 at mitotic exit impairs the expression of hundreds of genes, mostly downregulated, enriched on functions related to tissue growth and development. Rad21 binds the promoter of this group of genes. Remarkably, we uncover a direct interaction during the M-G1 transition between Rad21 and Cdk9, the kinase component of transcription elongation factor b (pTEFb) complex. Rad21 loss impairs Cdk9 chromatin association, reducing active-elongating RNAPol2 at down-regulated genes. Overall, preserving cohesin across mitosis enables post-mitotic transcriptional reactivation via Cdk9, establishing tissue-specific expression programs. - Source: PubMed
Publication date: 2026/09/16
Contreras-Pérez AidaEspinosa HéctorSayago Estrella IsabelBasu AvikEmili AndrewBlower Michael DPerea-Resa Carlos - Arginine vasopressin maintains water homeostasis by regulating epithelial water permeability through complex transcriptional mechanisms in kidney collecting duct cells. Although CTNNB1 (β-catenin) functions as a transcriptional coregulator in vasopressin-responsive gene transcription, its role remains poorly understood. To identify CTNNB1-dependent components mediating the vasopressin-responsive transcription, we profiled transcriptomic changes following Ctnnb1 knockdown in mouse kidney collecting duct cells using RNA sequencing (RNA-Seq). RNA-Seq and promoter enrichment analyses identified bromodomain-containing proteins (TRIM28, TRIM33, BRD4, CREBBP, and EP300) as components of a CTNNB1-dependent complex regulating RNA Polymerase II (Pol II) activity. Biochemical analyses revealed physical interactions between TRIM28, CTNNB1, Pol II, and CDK9. Functionally, Trim28 knockdown blunted vasopressin-induced expression of the gene. Quantitative genomic binding assays demonstrated that TRIM28 is required for robust genomic occupancy and stabilization of Pol II at the transcription start site of . Additionally, dynamic formation of phase-separated nuclear TRIM28 condensates in response to vasopressin suggests that TRIM28-associated machinery functions at specialized chromatin hubs. These findings reveal that TRIM28 facilitates Pol II recruitment, pause release, and elongation upon vasopressin stimulation. Our study establishes the CTNNB1-TRIM28 machinery as a critical transcriptional scaffold that controls Pol II dynamics and chromatin structure, thereby driving osmotic water reabsorption and urine concentration. - Source: PubMed
Publication date: 2026/09/15
Jang Hyo-JuPark EuijungJung Hyun JunKwon Tae-Hwan - Melanoma, a skin cancer with the highest mortality rate, poses a significant medical challenge. Despite the revolution in the treatment of this cancer brought about by the development of immunotherapy and targeted therapies using BRAF/MEK inhibitors, the complex mutation profile and the development of drug resistance compel researchers to seek new solutions. Cyclin-dependent kinases (CDKs), a group of enzymes regulating fundamental processes in every eukaryotic cell, are generating significant interest in the context of potential targeted therapies for melanoma. The best-studied CDKs, responsible for controlling specific phases of the cell-cycle, have been extensively described in the literature, and their inhibition is increasingly used as a treatment for various cancers. However, in addition to the classic cell-cycle CDKs, CDKs regulating transcription can also be distinguished. Other family members responsible for tissue-specific processes are commonly referred to as atypical or untypical CDKs. These include CDK5, which plays a critical role in the nervous system. In recent years, a growing body of research has focused on the role of transcriptional and atypical CDKs in the progression of cancers, including melanoma. However, their precise function remains unclear. This paper will provide an overview of the role of CDKs, other than cell cycle CDKs, in melanoma development and provide a comprehensive understanding of their potential use in future targeted therapies. The advantages and disadvantages of inhibiting these kinases in melanoma therapy will be discussed, as well as the synergies with various molecular pathways analyzed to date. - Source: PubMed
Publication date: 2026/08/22
Kaszubski JonatanGagat MaciejWawrzyniak AgataŻuryń Agnieszka - Functional magnetic resonance imaging (fMRI) has revealed abnormal brain activity patterns in stroke patients, yet the genetic correlates underlying functional homotopy - defined as synchronized spontaneous activity between bilateral homologous brain regions - remain poorly characterized. This study investigates the genetic basis of voxel-mirrored homotopic connectivity (VMHC) abnormalities in stroke patients. - Source: PubMed
Publication date: 2026/08/26
Chen Ri-BoHe Yu-XuanHuang XinWang Chang